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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Central retinal vein occlusion (CRVO) is one of the common causes of visual loss. The main reasons for decreased vision are development of macular edema, macular ischemia and neovascular glaucoma. The introduction of anti-vascular endothelial growth factor (VEGF) drugs for CRVO in 2005 demonstrated marked improvement in visual acuity, macular edema and ocular neovascularization. However, the absence of clear guidelines for the treatment of CRVO presents a genuine therapeutic challenge. In a national study conducted among the Israeli society of retinal specialists (personal communication), it was found that most of these specialists would recommend intravitreal anti-VEGF drug injection immediately upon the diagnosis of macular edema in non-ischemic CRVO with visual acuity of 6/15 or less. Only 21% would recommend this treatment in ischemic CRVO with visual acuity of 6/60 or less, if no macular edema exists. After the edema resolves, 94% would follow-up the patients by imaging with optical coherent tomography every 4-6 weeks, and recommend further treatment accordingly. Large prospective controlled studies are warranted in order to address the important issues of when to start anti-VEGF treatment for CRVO, when to withhold treatment, and recommended treatment intervals.
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PMID:[The use of anti-angiogenic drugs for central retinal vein occlusion]. 2081 99

Central retinal vein occlusion (CRVO) remains one of the most common retinal vascular disorders that may lead to blindness. The etiology is unknown, however, predisposing factors such as hypertension, diabetes, atherosclerosis and hypercoagulable states have all been described. Local ophthalmic illnesses such as open angle glaucoma, ocular trauma and orbital infections have also been suggested as causative. CRVO can be subdivided into two clinical types, ischemic and non-ischemic. The non-ischemic type comprises the milder form of the disease with partial venous obstruction and good visual outcome. Ischemic CRVO is the severe form and is associated with visual loss, because of nearly total retinal vein obstruction and poor perfusion to retina. In addition, patients with ischemic CRVO may end up with additional complications such as neovascular glaucoma that may lead to blindness. Over 90% of CRVO occurs in patients > 65 years. The presenting symptom is a sudden painless mono-ocular decrease in visual acuity which could result from macular edema, ischemia, or intraocular bleeding. Ophthalmoscopic examination reveals macular edema, retinal bleeding (more peripheral), tortuous vein dilatation and swollen disc. Current treatment modalities include systemic use of anticoagulation drugs, local treatments including laser, intravitreal injection of anti-vascular endothelial growth factor and surgery (vitrectomy). This review presents the current therapeutic modalities in CRVO.
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PMID:[Treatment modalities in central retinal vein occlusion]. 2081

Central retinal vein occlusion (CRVO) is an intractable disease that causes visual acuity loss with retinal ischemia, hemorrhage, and edema. In this study, we developed an experimental CRVO model in mice and evaluated the therapeutic potential of the pleiotropic peptide adrenomedullin (ADM) and its receptor activity-modifying protein 2 (RAMP2). The CRVO model, which had phenotypes resembling those seen in the clinic, was produced by combining i.p. injection of Rose bengal, a photoactivator dye enhancing thrombus formation, with laser photocoagulation. Retinal vascular area, analyzed using fluorescein angiography and fluorescein isothiocyanate-perfused retinal flat mounts, was decreased after induction of CRVO but gradually recovered from day 1 to 7. Measurements of retinal thickness using optical coherence tomography and histology revealed prominent edema early after CRVO, followed by gradual atrophy. Reperfusion after CRVO was diminished in Adm and Ramp2 knockout (KO) mice but was increased by exogenous ADM administration. CRVO also increased expression of a coagulation factor, oxidative stress markers, and a leukocyte adhesion molecule in both wild-type and Adm KO mice, and the effect was more pronounced in Adm KO mice. Using retinal capillary endothelial cells, ADM was found to directly suppress retinal endothelial injury. The retinoprotective effects of the Adm-Ramp2 system make it a novel therapeutic target for the treatment of CRVO.
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PMID:Development of a Novel Model of Central Retinal Vascular Occlusion and the Therapeutic Potential of the Adrenomedullin-Receptor Activity-Modifying Protein 2 System. 3065 46

Retinal oximetry imaging of retinal blood vessels measures oxygen saturation of hemoglobin. The imaging technology is non-invasive and reproducible with remarkably low variability on test-retest studies and in healthy cohorts. Pathophysiological principles and novel biomarkers in several retinal diseases have been discovered, as well as possible applications for systemic and brain disease. In diabetic retinopathy, retinal venous oxygen saturation is elevated and arteriovenous difference progressively reduced in advanced stages of retinopathy compared with healthy persons. This correlates with pathophysiology of diabetic retinopathy where hypoxia stimulates VEGF production. Laser treatment and vitrectomy both improve retinal oximetry values, which correlate with clinical outcome. The oximetry biomarker may allow automatic measurement of severity of diabetic retinopathy and predict its response to treatment. Central retinal vein occlusion is characterized by retinal hypoxia, which is evident in retinal oximetry. The retinal hypoxia seen on oximetry correlates with the extent of peripheral ischemia, visual acuity and thickness of macular edema. This biomarker may help diagnose and measure severity of vein occlusion and degree of retinal ischemia. Glaucomatous retinal atrophy is associated with reduced oxygen consumption resulting in reduced arteriovenous difference and higher retinal venous saturation. The oximetry findings correlate with worse visual field, thinner nerve fiber layer and smaller optic disc rim. This provides an objective biomarker for glaucomatous damage. In retinitis pigmentosa, an association exists between advanced atrophy, worse visual field and higher retinal venous oxygen saturation, lower arteriovenous difference. This biomarker may allow measurement of severity and progression of retinitis pigmentosa and other atrophic retinal diseases. Retinal oximetry offers visible light imaging of systemic and central nervous system vessels. It senses hypoxia in cardiac and pulmonary diseases. Oximetry biomarkers have been discovered in Alzheimer's disease and multiple sclerosis and oxygen levels in the retina correspond well with brain.
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PMID:Retinal oximetry: Metabolic imaging for diseases of the retina and brain. 3099 27

Central retinal vein occlusion (CRVO) causes macular edema and subsequent vision loss and is common in people with diseases such as arteriosclerosis and hypertension. Various treatments for CRVO-associated macular edema have been trialed, including laser photocoagulation, with unsatisfactory results. However, when the important pathogenic role of vascular endothelial growth factor (VEGF) in macular edema was identified, the treatment of CRVO was revolutionized by anti-VEGF therapy. However, despite the success of intraocular injection of anti-VEGF agents in many patients with CRVO, some patients continue to suffer from refractory or recurring edema. In addition, the expression of inflammatory cytokines increases over time, causing more severe inflammation and a condition that is increasingly resistant to anti-VEGF therapy. This indicates that the pathogenesis of macular edema in CRVO is more complex than originally thought and may involve factors or cytokines associated with inflammation and ischemia other than VEGF. CRVO is also associated with leukocyte abnormalities and a gradual reduction in retinal blood flow velocity, which increase the likelihood of it developing from the nonischemic type into the more severe ischemic type; in turn, this results in excessive VEGF expression and subsequent neovascular glaucoma. Here, we review the role of different factors and cytokines involved in CRVO pathogenesis and propose a mechanism that holds promise for the development of novel therapies.
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PMID:Cytokines and Pathogenesis of Central Retinal Vein Occlusion. 3312 Oct 94